| Accelerated wound healing mediated by activation of Toll-like receptor 9. | |
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MedLine Citation:
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PMID: 20946144 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Wound healing is mediated through complex interactions between circulating immune cells and local epithelial and endothelial cells. Elements of the innate immune system are triggered when Toll-like receptors (TLR) are stimulated by their cognate ligands, and previous studies suggest that such interactions can accelerate wound healing. This work examines the effect of treating excisional skin biopsies with immunostimulatory CpG oligodeoxynucleotides (ODN) that trigger via TLR9. Results indicate that CpG (but not control) ODN accelerate wound closure and reduce the total wound area exposed over time by >40% (p<0.01). TLR9 knockout mice, a strain unresponsive to the immunomodulatory effects of CpG stimulation, are unresponsive to ODN treatment and exhibit a general delay in healing when compared with wild-type mice. CpG ODN administration promoted the influx of macrophages to the wound site and increased the production of vascular endothelial growth factor, expediting neovascularization of the wound bed (p<0.01 for both parameters). Stimulation via TLR9 thus represents a novel strategy to accelerate wound healing. |
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Authors:
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Takashi Sato; Masaki Yamamoto; Takeshi Shimosato; Dennis M Klinman |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-13 |
Journal Detail:
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Title: Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society Volume: 18 ISSN: 1524-475X ISO Abbreviation: Wound Repair Regen Publication Date: 2010 Nov-Dec |
Date Detail:
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Created Date: 2010-12-24 Completed Date: 2011-05-31 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 9310939 Medline TA: Wound Repair Regen Country: United States |
Other Details:
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Languages: eng Pagination: 586-93 Citation Subset: IM |
Copyright Information:
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© 2010 by the Wound Healing Society. |
Affiliation:
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Cancer and Inflammation Program, National Cancer Institute, Frederick, Maryland 21702, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adjuvants, Immunologic
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pharmacology Animals Antigens, CD31 / metabolism Biopsy Female Macrophages / metabolism Mice Mice, Inbred BALB C Mice, Knockout Neovascularization, Physiologic Oligodeoxyribonucleotides / pharmacology Skin / metabolism, pathology Toll-Like Receptor 9 / physiology* Vascular Endothelial Growth Factor A / biosynthesis Wound Healing / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Adjuvants, Immunologic; 0/Antigens, CD31; 0/CPG-oligonucleotide; 0/Oligodeoxyribonucleotides; 0/Tlr9 protein, mouse; 0/Toll-Like Receptor 9; 0/Vascular Endothelial Growth Factor A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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